Artikel
Impact of CPAP on renal function in hypertensive patients with obstructive sleep apnea
Einfluß von CPAP auf die Nierenfunktion bei hypertensiven Patienten mit obstruktiver Schlafapnoe
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Veröffentlicht: | 10. August 2005 |
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Background: In addition to hypertension patients with obstructive sleep apnea (OSA) often suffer from other risk factors for renal dysfunction such as diabetes, hyperlipidemia, nocturnal hypoxemia, and increased sympathetic nerve activity. Aim of this ongoing study is to examine the influence of continuous positive airway pressure therapy (CPAP) on renal function in OSA patients with and without hypertension.
Methods: Up to now 25 patients with confirmed OSA have been treated with CPAP. Parameters of renal function (serum creatinine, endogenous creatinine clearance, spot urine albumin/creatinine-ratio) were correlated to polysomnographic results and reevaluated after 6 months.
Results: All degrees of OSA have been observed with a mean apnea/hpopnea index (AHI) of 31.2+/-24.3/h (range 7.8 - 103.0). Mean patient age was 61.5+/8.7 years. In 4 patients CPAP proved to be ineffective. In 16 of the remaining 21 patients hypertension (RR > 140/90 mmHg or use of antihypertensive drugs) was present. There were no significant differences between the groups of hypertensive and normotensive patients regarding age, gender, degree of OSA, changes of lipid and glucose metabolism and the parameters of renal function at the beginning of the study. After 6 months of CPAP therapy serum creatinine decreased (1.05+/-0.19 to 0.93+/-0.16 mg/dL, p 0.010) only in the patients with hypertension, whereas it remained unchanged in normotensive and ineffectively treated patients. Changes of serum creatinine were not associated to initial levels or the course of any parameter of OSA (AHI, arousal index, sleep stages, oxygen saturation). Albuminuria did not change with CPAP therapy in hypertensive, normotensive, and all effectively treated patients.
Conclusion: Our results suggest beneficial effects of CPAP therapy on renal function in OSA patients with hypertension. Further prospective studies are needed to elucidate the underlying pathophysiologic mechanism.